Texas Tech University

Brian Reilly

Associate Professor

Email: brian.reilly@ttu.edu

Phone: 1 (806) 834-2255

Reilly

About Dr. Reilly:

Dr. Reilly did graduate work at McGill University and received his Ph.D. from the University of New Mexico, School of Medicine, and was a National Institutes of Health (NIH) postdoctoral fellow.  Since joining the faculty at TTU, he has served on over 30 NIH study panels (co-chaired two), three NSF panels and has been an ad hoc reviewer of multiple NSF and USDA grants.  He currently serves on the Review Board for the Journal of Molecular Immunology and is an Associate Editor for Frontiers in Immunology.  He has over 25 publications in peer-reviewed Immunology journals.  As a Principal Investigator, he has received seven grants from the NIH, one from the Arthritis Foundation of Canada, and two Major Instrumentation grants.  His laboratory is currently funded by Island Oil Explorations, and he is a collaborator or co-investigator on two grants from the NIH. 

In addition to teaching undergraduate and graduate courses in Immunology and Host Defense, his laboratory investigates the genetic factors contributing to autoimmune disease, particularly Systemic Lupus Erythematosus (SLE).  The cause of SLE is poorly understood but is generally considered to be initiated by an attack on the tissues of our body by auto-reactive antibodies and T lymphocytes.  Epidemiological studies, utilizing large cohorts of individuals from different ethnic backgrounds, have shown that individuals with inherited deficiencies of the complement proteins C1q or C4 have an extremely high risk of developing SLE, 90% and 80%, respectively.  Despite high penetrance, the physiological basis for this disease association is lacking.  His laboratory has previously contributed important information on the structure and function of C4 and of CD35, the cellular receptor that recognizes and binds C4.  More recently, his laboratory has demonstrated that T cells expressing CD35 are unique regulatory lymphocytes whose function appears to be controlled by C4, and it was discovered that patients with active SLE express an aberrant form of C4 that interacts poorly with this receptor.  Currently, the effect of C4 on this novel T cell is being actively investigated utilizing tissue samples from both normal and SLE patients with an eye to the development of immunotherapy for autoimmune disease. 

Department of Biological Sciences

  • Address

    Department of Biological Sciences, Texas Tech University, Box 43131 Lubbock, TX 79409
  • Phone

    806.742.2715
  • Email

    biology@ttu.edu